Monthly Archives: May 2011

Polygonum bistorta

Botanical Name :Polygonum bistorta or Persicaria bistorta
Family: Polygonaceae
Genus: Persicaria
Species: P. bistorta
Kingdom: Plantae
Order: Caryophyllales
Synonyms: Persicaria bistorta (L.) Samp., Polygonum ampliusculum Gand., Polygonum bistorta L., Polygonum bourdinii Gand., Polygonum carthusianorum Gand., Polygonum ellipticum Willd. ex Spreng., Polygonum pilatense Gand.

Common Name : Bistort or Common Bistort

Habitat :Persicaria bistorta (Bistort or Common Bistort) is a herbaceous flowering plant found throughout Europe. The generic placement of this species is in flux. While treated here as in Persicaria, it has also been placed in Polygonum or Bistorta.

Description:
Plants bloom late spring into mid summer, producing tall stems ending in single terminal racemes that are club-like spikes of pink-rose colored flowers. The racemes are about 2 cm thick and 5-9 cm long and end 1 meter tall,upright growing stems. Plants grow in moist soils and under dry conditions go dormant, losing their foliage until adequate moisture exists again. This species is grown as an ornamental garden plant, especially the form ‘Superba’ which has larger, more showy flowers. Typically alpine plants growing from short, thick rhizomes that branch. The foliage is normally basal with a few smaller leaves produced near the lower end of the flowering stems. The leaves are oblong-ovate or triangular-ovate in shape and narrow at the base. The petioles are broadly winged.
CLICK & SEE THE PICTURES
The Latin name “bistorta” refers to the twisted appearance of the root. In Northern England the plant was used to make a bitter pudding in Lent from a combination of the plant’s leaves, oatmeal, egg and other herbs. It is the principal ingredient of dock pudding or Easter-Ledge Pudding.  The root of Bistort can be used to produce an astringent that was used in medicine.

Numerous other vernacular names have been recorded for the species in historical texts, though none is used to any extent. Many of the following refer to the plant’s use in making puddings: Adderwort, Dragonwort, Easter giant, Easter ledger, Easter ledges, Easter magiant, Easter man-giant, Gentle dock, Great bistort, Osterick, Oysterloit, Passion dock, Patience dock (this name is also used for Rumex patientia), Patient dock, Pink pokers, Pudding grass, Pudding dock, Red legs, Snakeweed, Twice-writhen, Water ledges.

Medicinal Uses:
Roots and leaves were used to counteract poisons and to treat malaria and intermittent fevers.  Dried and powdered it was applied to cuts and wounds to staunch bleeding, and a decoction in wine was taken for internal bleeding and diarrhea (especially in babies).  It was also given to cause sweating and drive out the plague, smallpox, measles and other infectious diseases.  Bistort is rich in tannins and one of the best astringents.  Taken internally, it is excellent for bleeding, such as from nosebleeds, heavy periods and wounds, and for diarrhea and dysentery.  Since it reduces inflammation and mucous secretions it makes a good remedy for colitis and for catarrhal congestion.  It was originally recommended in 1917 as a treatment for debility with a tendency towards tuberculosis.  It has also been used externally for pharyngitis, stomatitis, vaginal discharge, anal fissure, purulent wounds, hemorrhoids, mouth ulcers and gum disease.  Comes well with Geranium maculatum.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:

http://en.wikipedia.org/wiki/Persicaria_bistorta

http://www.herbnet.com/Herb%20Uses_AB.htm

Enhanced by Zemanta

Hypercalcaemia

Definition:-

Calcium is a mineral that’s vital for the development of healthy bones and teeth – 99 per cent of the calcium in our bodies is found here. It’s also needed for muscle contraction, regulation of the heartbeat and formation of blood clots. A long-term shortage of calcium can lead to osteoporosis (brittle-bone disease).

The four pea-sized parathyroid glands (found at the front of the neck) are responsible for regulating the body’s calcium levels. These small glands, which are embedded in the tissue of the thyroid gland in the neck, detect fluctuations in the level of calcium in the blood.

CLICK & SEE

There are times when this delicate balance is upset and too much calcium enters the blood. If levels rise too much, the glands decrease the secretion of the parathyroid hormone (PTH) and calcium levels return to normal again.
click to see
Hypercalcaemia  is an elevated calcium level in the blood. (Normal range: 9–10.5 mg/dL or 2.2–2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a diagnosis should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

click to see

Symptoms:-
There is a general mnemonic for remembering the effects of hypercalcaemia: “groans (constipation), moans (psychic moans (e.g., fatigue, lethargy, depression)), bones (bone pain, especially if PTH is elevated), stones (kidney stones), and psychiatric overtones (including depression and confusion).”

Other symptoms can include fatigue, anorexia, nausea,abdominal pain, weightloss,loss of appetite, vomiting,constipation, pancreatitis and increased urination.

Abnormal heart rhythms can result, and ECG findings of a short QT interval and a widened T wave suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.

Peptic ulcers may also occur.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result.

Causes:-
One of the commonest causes of hypercalcaemia is cancer. Up to 20% of people with cancer have high calcium levels, especially with cancers of the breast, lung, head and neck, and certain blood cancers.

Abnormal parathyroid gland function:
*primary hyperparathyroidism
*solitary parathyroid adenoma
*primary parathyroid hyperplasia
*parathyroid carcinoma
*multiple endocrine neoplasia (MEN)
*familial isolated hyperparathyroidism
*lithium use
*familial hypocalciuric hypercalcaemia/familial benign hypercalcaemia

Malignancy:
*solid tumour with metastasis (e.g. breast cancer or classically squamous cell carcinoma, which can be PTHrP-mediated)
*solid tumour with humoral mediation of hypercalcaemia (e.g. lung cancer [in turn, most commonly of the small cell lung cancer type] or kidney cancer, pheochromocytoma)
*haematologic malignancy (multiple myeloma, lymphoma, leukaemia)

Vitamin-D metabolic disordershyper:
*vitaminosis D (vitamin D intoxication)
*elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases)
*idiopathic hypercalcaemia of infancy
*rebound hypercalcaemia after rhabdomyolysis

Disorders related to high bone-turnover rateshyperthyroidism:
*prolonged immobilization
*thiazide use
*vitamin A intoxication
*Paget’s disease of the bone
*multiple myeloma

Renal failure
*severe secondary hyperparathyroidism:
*aluminium intoxication
*milk-alkali syndrome

Risk Factors:
An overproduction of PTH may also responsible for hypercalcaemia; this is often caused by a tumour in one or more of the parathyroid glands. Excess production of PTH may occur to compensate for a malfunction in one of the body’s other calcium-balancing mechanisms; for example, when the kidneys aren’t working properly or when there’s a deficiency of vitamin D.

Women over the age of 50 are most likely to have hypercalcemia, usually due to primary hyperparathyroidism.

Diagnosis:
Hypercalcaemia is diagnosed by laboratory tests including: serum calcium, albumin, phosphate, alkaline phosphate, BUN, creatinine, electrolytes and PTH level. These investigations assist in diagnosing the cause of hypercalcaemia and give a baseline indication of renal function. Urinary calcium should be measured as hypercalciuria may be detected. Other investigations may include an ECG and radiology examinations such as x-ray or bone scans which may show bone metastases

Treatment:
The treatment of hypercalcaemia is determined by the underlying disease, the degree of the hypercalcaemia and the patient’s clinical presentation. The aim of treatment is directed at decreasing serum calcium levels by increasing urinary excretion of calcium and decreasing bone resorption of calcium. Immobilization should be avoided as inactivity will cause an increase in bone resorption of calcium. The level of activity will be appropriate for the patient’s physical condition and other measures such as pain control may need to be considered prior to undertaking any physical activities. A review of the patient’s medications will need to be considered. Drugs that inhibit urinary calcium excretion, such as thiazide diuretics, should be ceased. NSAID and H2-receptor drugs, such as Ranitidine which decrease renal blood flow, should also be avoided if possible. Any calcium, Vitamin A and D supplements should also be ceased. Dietary restrictions of calcium have not been proven to be of any benefit to patients that are hypercalcaemic, or at risk of hypercalcaemia. Currently there is no data to suggest that hypercalcaemia has been attributed to food. However, some dietary supplements can cause abnormally hight levels of calcium in the blood. Patients with chronic renal failure are at risk of becoming hypercalacemic due to calcium intake.

This is due to decreased urine production, in combination with high calcium intake). Intravenous fluids (0.9% sodium chloride) will be administered to rehydrate the patient, the volume of fluid given will depend on the extent of the patients dehydration and cardiovascular and renal functions. At least 4-6 litres of saline on day 1, and 3-4 litres for several days thereafter is usual. Diuretics such as frusemide may also be given. Repeat blood tests should be taken several hours after treatment and reassessed. Cardiac status and urinary output should also be assessed, thus a strict fluid balance chart should be maintained on the patient. Oral phosphates, which inhibit bone resorption, may be administered. Diarrhoea is a common side effect and may lead to non-compliance. Bisphosphonates, which are given intravenously, inhibit osteoclast activity that contributes to bone resorption may also be administered. The two most common drugs used are Pamidronate/Aredia (60-90mg IV over 2 hours) and Zoledronic Acid/Zometa (4mg IV over 15 minutes). Both of these agents are generally well tolerated with limited side effects such as mild fever and irritation at the infusion site.

Prognosis:
The prognosis of hypercalcaemia depends upon the cause of increased calcium levels. When the underlying cause is treatable and the treatment is initiated promptly, hypercalcaemia can have a good prognosis. However, when associated with malignancy that has progressed into development of hypercalcemia, prognosis is poor. Hypercalcaemia is potentially fatal. Early diagnosis is important, as the cause of high blood calcium is usually identified and treated to avoid long-term complications. Signs and symptoms may be confused with those of end stage disease in terminal patients. In some patients, symptoms may be non-specific and have a slow onset.Some examples of these are:
•Anorexia
•Weakness
•Nausea
•Vomiting
•Constipation

In other cases, symptoms such as dehydration, renal failure and coma may develop very quickly resulting from very rapidly rising calcium levels. This may result in a life threatening situation. Symptoms do not always correlate with serum calcium levels. These must be closely compared with an in-depth patient history, examination and laboratory report. Signs and symptoms of hypercalcaemia can be numerous and nonspecific. They depend on the underlying cause and how quickly the calcium level rises. Mild hypercalcaemia may be asymptomatic but as the calcium levels rise, the symptoms begin to appear in all body systems. Some non-specific findings associated with hypercalcaemia include: decreased heart rate, hypertension, proximal muscle weakness (chronic hypercalcaemia), bony tenderness, increased tendon reflexes, unwanted tongue movements, dehydration and even coma.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/hypercalcaemia1.shtml

http://en.wikipedia.org/wiki/Hypercalcaemia

http://www.virtualmedicalcentre.com/symptoms.asp?sid=31&title=Hypercalcaemia#C3

http://erc.endocrinology-journals.org/content/12/3/549.full

Enhanced by Zemanta

Molar Pregnancy

Definition:
A molar pregnancy is one condition in a range of problems known as trophoblastic disease, where a pregnancy doesn’t grow as it should. It’s sometimes called a hydatiform mole.

There are two different types of molar pregnancy, which differ in how they form and how they need to be treated.

In a normal pregnancy, genetic material from the mother and father combines to form new life. In a molar pregnancy, this process goes wrong. In a complete molar pregnancy, the maternal chromosomes are lost, either at conception or while the egg was forming in the ovary, and only genetic material from the father develops in the cells. In a partial molar pregnancy, there is a set of maternal chromosomes but also two sets of chromosomes from the father (ie, double the normal paternal genetic material).

CLICK & SEE

The genotype is typically 46,XX (diploid) due to subsequent mitosis of the fertilizing sperm, but can also be 46,XY (diploid).  In contrast, a partial mole occurs when an egg is fertilized by two sperm or by one sperm which reduplicates itself yielding the genotypes of 69,XXY (triploid) or 92,XXXY (quadraploid).

Complete molar pregnancies develop as a mass of rapidly growing cells but without a foetus – it cannot therefore develop into a baby.
……
In a partial molar pregnancy, a foetus may start to develop but because of the imbalance in genetic material, it’s always abnormal and can’t survive beyond the first three months of pregnancy.

A molar pregnancy is often harmless, but if untreated can keep on growing and become invasive, spreading to the organs around it, or even further afield to the lungs, liver or brain. Very rarely, in two to three per cent of cases, it may become malignant. These cancerous types of trophoblastic disease are called choriocarcinoma and placental site trophoblast tumours.

Symptoms:
As the mole grows faster than a normal foetus would, the abdomen may become larger more quickly than would be expected for the dates of the pregnancy. The woman may experience abdominal pain, and also severe nausea and vomiting (hyperemesis).

Bleeding from the vagina is another common warning sign that things are not as they should be. Symptoms similar to pre-eclampsia – high blood pressure, protein in the urine, swelling of the feet and legs – may also occur in the first trimester or early in the second.

Most molar pregnancies are diagnosed at the first ultrasound scan, which shows a mass of cells without the presence of a foetus in a complete molar pregnancy or an abnormal non-viable foetus and placenta in a partial mole.

A woman with a hydatidiform mole often feels pregnant and has symptoms such as morning sickness, probably because the cells of the molar pregnancy produce the pregnancy hormone hCG (human chorionic gonadotrophin). This is also the hormone that is used in a pregnancy test, so she may have a positive result. Some women have no pregnancy symptoms (as with many normal pregnancies). — but most molar pregnancies cause specific signs and symptoms, including:

*Dark brown to bright red vaginal bleeding during the first trimester

*Severe nausea and vomiting

*Vaginal passage of grape-like cysts

*Rarely, pelvic pressure or pain

If you experience any signs or symptoms of a molar pregnancy, consult your health care provider. He or she may detect other signs of a molar pregnancy, such as:

*Rapid uterine growth — the uterus is too large for the stage of pregnancy

*High blood pressure

*Preeclampsia — a condition that causes high blood pressure and protein in the urine after 20 weeks of pregnancy

*Ovarian cysts

*Anemia

*Overactive thyroid (hyperthyroidism)

Causes:
A molar pregnancy is caused by an abnormally fertilized egg. Human cells normally contain 23 pairs of chromosomes. One chromosome in each pair comes from the father, the other from the mother. In a complete molar pregnancy, all of the fertilized egg’s chromosomes come from the father. Shortly after fertilization, the chromosomes from the mother’s egg are lost or inactivated and the father’s chromosomes are duplicated. The egg may have had an inactive nucleus or no nucleus.

In a partial or incomplete molar pregnancy, the mother’s chromosomes remain but the father provides two sets of chromosomes. As a result, the embryo has 69 chromosomes, instead of 46. This can happen when the father’s chromosomes are duplicated or if two sperm fertilize a single egg.

It remains unclear why a hydatidiform mole develops. However, there are a number of possible reasons, including defects in the egg, maternal nutritional deficiencies and uterine abnormalities. Women under 20 or over 40 are at higher risk.

Having a diet that’s low in protein, folic acid and carotene also increases the risk of a molar pregnancy. The number of times a women has been pregnant, however, doesn’t influence her risk.

Risk Factors:
Up to an estimated 1 in every 1,000 pregnancies is molar. Various factors are associated with molar pregnancy, including:

*Maternal age. A molar pregnancy is more likely for a woman older than age 35 or younger than age 20.

*Previous molar pregnancy. If you’ve had one molar pregnancy, you’re more likely to have another. The risk of a repeat molar pregnancy is 1 in 100.

*Some ethnic groups. Women of Southeast Asian descent appear to have a higher risk of molar pregnancy.

Diagnosis:
Molar pregnancies usually present with painless vaginal bleeding in the fourth to fifth month of pregnancy. The uterus may be larger than expected, or the ovaries may be enlarged. There may also be more vomiting than would be expected (hyperemesis). Sometimes there is an increase in blood pressure along with protein in the urine. Blood tests will show very high levels of human chorionic gonadotropin (hCG).

The diagnosis is strongly suggested by ultrasound (sonogram), but definitive diagnosis requires histopathological examination. On ultrasound, the mole resembles a bunch of grapes (“cluster of grapes” or “honeycombed uterus” or “snow-storm”). There is increased trophoblast proliferation and enlarging of the chorionic villi. Angiogenesis in the trophoblasts is impaired as well.

Sometimes symptoms of hyperthyroidism are seen, due to the extremely high levels of hCG, which can mimic the normal Thyroid-stimulating hormone (TSH).

Treatment :
Once it has been established that a woman is carrying a hydatidiform mole rather than a healthy foetus, suction evacuation is used to remove the pregnancy from the womb. This is curative in about four out of five molar pregnancies.

It’s then important to monitor the woman’s progress and repeatedly measure human chorionic gonadotropin (hCG) to be sure that everything settles back down to a normal, non-pregnancy level.

About 15 per cent of women who have had a complete molar pregnancy and 0.5 per cent of those with a partial molar pregnancy will require additional treatment, either because hCG levels hit a plateau or start to rise again, or because of persistent heavy vaginal bleeding.

Further treatment may involve the use of chemotherapy (usually methotrexate combined with folinic acid), especially if there’s any concern about invasive or malignant disease.

Complications:
After a molar pregnancy has been removed, molar tissue may remain and continue to grow. This is called persistent gestational trophoblastic disease (GTD). It occurs in about 10 percent of women after a molar pregnancy — usually after a complete mole rather than a partial mole. One sign of persistent GTD is an HCG level that remains high after the molar pregnancy has been removed. In some cases, an invasive mole penetrates deep into the middle layer of the uterine wall, which causes vaginal bleeding. Persistent GTD can nearly always be successfully treated, most often with chemotherapy. Another treatment option is removal of the uterus (hysterectomy).

Rarely, a cancerous form of GTD known as choriocarcinoma develops and spreads to other organs. Choriocarcinoma is usually successfully treated with multiple cancer drugs.

Prognosis:
More than 80% of hydatidiform moles are benign. The outcome after treatment is usually excellent. Close follow-up is essential. Highly effective means of contraception are recommended to avoid pregnancy for at least 6 to 12 months.

In 10 to 15% of cases, hydatidiform moles may develop into invasive moles. This condition is named persistent trophoblastic disease (PTD). The moles may intrude so far into the uterine wall that hemorrhage or other complications develop. It is for this reason that a post-operative full abdominal and chest x-ray will often be requested.

In 2 to 3% of cases, hydatidiform moles may develop into choriocarcinoma, which is a malignant, rapidly-growing, and metastatic (spreading) form of cancer. Despite these factors which normally indicate a poor prognosis, the rate of cure after treatment with chemotherapy is high.

Over 90% of women with malignant, non-spreading cancer are able to survive and retain their ability to conceive and bear children. In those with metastatic (spreading) cancer, remission remains at 75 to 85%, although their childbearing ability is usually lost.

Prevention:
Following successful treatment, most women can have children if they wish. However, it’s strongly recommended that a woman who has had a molar pregnancy doesn’t become pregnant again for 12 months. Although the likelihood is small, there’s a real risk of malignant disease developing and the increase in pregnancy hormones this would cause can’t be distinguished from those of a real pregnancy. Consequently, good contraception is required, as is regular monitoring by a hospital specialist.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/hydatidiformmole1.shtml

http://www.mayoclinic.com/health/molar-pregnancy/DS01155

http://en.wikipedia.org/wiki/Hydatidiform_mole

http://drugster.info/ail/pathography/375/

Enhanced by Zemanta

Cymopterus bulbosus

Botanical Name :Cymopterus bulbosus
Family :Apiaceae
Genus : Cymopterus Raf.
Species : Cymopterus bulbosus A. Nelson
Kingdom : Plantae
Subkingdom :Tracheobionta
Superdivision : Spermatophyta
Division : Magnoliophyta
Class : Magnoliopsida
Subclass : Rosidae
Order : Apiales

Common Name :Biscuit Root

Habitat :South-western N. America – Wyoming to Texas and New Mexico. Dry hills and plains at elevations of 1200 – 2100 metres.

Description:
Cymopterus bulbosus is a perennial hurb. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects.The plant is self-fertile.
CLICK & SEE THE PICTURES……

The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and requires well-drained soil.The plant prefers acid, neutral and basic (alkaline) soils..It can grow in semi-shade (light woodland) or no shade.It requires dry or moist soil.

Propagation
Seed – we have no information on this species but suggest sowing the seed in a cold frame as soon as it is ripe if this is possible. Sow stored seed as early in the year as possible in a greenhouse. As soon as they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for at least their first winter. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Division in spring or autumn might be possible

Edible Uses
Edible Parts: Condiment;  Leaves;  Root.

The root can be eaten raw, cooked or dried for later use. The dried leaves are used as a flavouring[61, 105, 177]. A celery flavouring. Leaves – cooked

Medicinal Uses:
The plant has been eaten as a stomach medicine.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Sources:

http://www.pfaf.org/user/Plant.aspx?LatinName=Cymopterus%20bulbosus

http://www.swcoloradowildflowers.com/Pink%20Enlarged%20Photo%20Pages/cymopterus%20bulbosus%20and%20constancei.htm

http://plants.usda.gov/java/profile?symbol=CYBU

http://www.herbnet.com/Herb%20Uses_AB.htm

Enhanced by Zemanta

Hydrocephalus

Definition:
Hydrocephalus, also known as “water on the brain,” is a medical condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain  and is an excessive amount of fluid that surrounds the brain and spinal cord called cerebrospinal fluid (or CSF).

This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, tunnel vision, and mental disability.The excess fluid can compress surrounding, fragile brain tissue, causing brain damage. Left untreated, hydrocephalus can be fatal. Hydrocephalus can also cause death.
CLICK & SEE THE PICTURES.....
Hydrocephalus is sometimes present at birth, although it may develop later. About 1 out of 500 children is born with the disorder. The outlook if you have hydrocephalus depends on how quickly the condition is diagnosed and whether any underlying disorders are present.

The name derives from the Greek words  hudro means “water”, and kephalos means “head”.

Symptoms:
The clinical presentation of hydrocephalus varies with chronicity. Acute dilatation of the ventricular system is more likely to manifest with the nonspecific signs and symptoms of increased intracranial pressure. By contrast chronic dilatation (especially in the elderly population) may have a more insidious onset presenting, for instance, with the Hakim triad.

Symptoms of increased intracranial pressure may include headaches, vomiting, nausea, papilledema, sleepiness or coma. Elevated intracranial pressure may result in uncal and/or cerebellar tonsill herniation, with resulting life threatening brain stem compression. For details on other manifestations of increased intracranial pressure:

The triad (Hakim triad) of gait instability, urinary incontinence and dementia is a relatively typical manifestation of the distinct entity normal pressure hydrocephalus (NPH). Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located).

The symptoms depend on the cause of the blockage, the person’s age, and how much brain tissue has been damaged by the swelling.

In infants with hydrocephalus, CSF builds up in the central nervous system, causing the fontanelle (soft spot) to bulge and the head to be larger than expected. Early symptoms may also include:

*Eyes that appear to gaze downward (Sundowning)
*Irritability
*Seizures
*Separated sutures
*Sleepiness
*Vomiting

Symptoms that may occur in older children can include:

*Brief, shrill, high-pitched cry
*Changes in personality, memory, or the ability to reason or think
*Changes in facial appearance and eye spacing
*Crossed eyes or uncontrolled eye movements
*Difficulty feeding
*Excessive sleepiness
*Headache
*Irritability, poor temper control
*Loss of bladder control (urinary incontinence)
*Loss of coordination and trouble walking
*Muscle spasticity (spasm)
*Slow growth (child 0–5 years)
*Slow or restricted movement
*Vomiting

Hydrocephalus produces different combinations of these signs and symptoms, depending on its cause, which also varies by age. For example, a condition known as normal pressure hydrocephalus, which mainly affects older people, typically starts with difficulty walking. Urinary incontinence often develops, along with a type of dementia marked by slowness of thinking and information processing.

Causes:
In hydrocephalus, CSF builds up and puts pressure on the brain, squashing the delicate tissues and causing the chambers or ventricles within the brain to swell. Without treatment damage or destruction of the brain tissues may occur.

Our brain is the consistency of gelatin, and it floats in a bath of cerebrospinal fluid. This fluid also fills large open structures, called ventricles, which lie deep inside your brain. The fluid-filled ventricles help keep the brain buoyant and cushioned.

Cerebrospinal fluid flows through the ventricles by way of interconnecting channels. The fluid eventually flows into spaces around the brain, where it’s absorbed into your bloodstream.

Keeping the production, flow and absorption of cerebrospinal fluid in balance is important to maintaining normal pressure inside your skull. Hydrocephalus results when the flow of cerebrospinal fluid is disrupted — for example, when a channel between ventricles becomes narrowed — or when your body doesn’t properly absorb this fluid.

There are two types of hydrocephalus:
Non-communicating hydrocephalus – the flow of CSF through the brain is blocked.
Communicating hydrocephalus - either too much CSF is produced, or it isn’t reabsorbed back into the tissues as it should be, so volume increases.

There are many causes of hydrocephalus and some of them are:
•Bleeding in the brain (for example if a baby is born very preterm)
•Congenital malformations (structural abnormalities that are present from birth)
•After infections in the brain
•Brain tumours
•Abnormalities in the blood vessels in the brain

Defective absorption of cerebrospinal fluid causes normal pressure hydrocephalus, seen most often in older people. In normal pressure hydrocephalus, excess fluid enlarges the ventricles but does not increase pressure on the brain. Normal pressure hydrocephalus may be the result of injury or illness, but in many cases the cause is unknown.

Risk Factors:
Premature infants have an increased risk of severe bleeding within the ventricles of the brain (intraventricular hemorrhage), which can lead to hydrocephalus.

Certain problems during pregnancy may increase an infant’s risk of developing hydrocephalus, including:
*An infection within the uterus
*Problems in fetal development, such as incomplete closure of the spinal column

Congenital or developmental defects not apparent at birth also can increase older children’s risk of hydrocephalus.

Other factors that increase your risk of hydrocephalus include:
*Lesions or tumors of the brain or spinal cord
*Central nervous system infections
*Bleeding in the brain
*Severe head injury

Complications:
The severity of hydrocephalus depends on the age at which the condition develops and the course it follows. If the condition is well advanced at birth, major brain damage and physical disabilities are likely. In less severe cases, with proper treatment, it’s possible to have a nearly normal life span and intelligence.

Congenital:
The cranial bones fuse by the end of the third year of life. For head enlargement to occur, hydrocephalus must occur before then. The causes are usually genetic but can also be acquired and usually occur within the first few months of life, which include 1) intraventricular matrix hemorrhages in premature infants, 2) infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and stenosis, and 5) Dandy-Walker malformation.

In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th percentile. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position.

The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in his surroundings. Later on, the upper eyelids become retracted and the eyes are turned downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous. Papilledema is absent but there may be reduction of vision. The head becomes so enlarged that the child may eventually be bedridden.

About 80-90% of fetuses or newborn infants with spina bifida—often associated with meningocele or myelomeningocele—develop hydrocephalus.

Acquired:
This condition is acquired as a consequence of CNS infections, meningitis, brain tumors, head trauma, intracranial hemorrhage (subarachnoid or intraparenchymal) and is usually extremely painful.

Effects:
Because hydrocephalus can injure the brain, thought and behavior may be adversely affected. Learning disabilities including short-term memory loss are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However the severity of hydrocephalus can differ considerably between individuals and some are of average or above-average intelligence. Someone with hydrocephalus may have motion and visual problems, problems with coordination, or may be clumsy. They may reach puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/hydrocephalus2.shtml

http://www.mayoclinic.com/health/hydrocephalus/DS00393

http://en.wikipedia.org/wiki/Hydrocephalus

Enhanced by Zemanta

Prickly Heat? Don’t Try Talc

Sweat (Hadise album)

Sweat (Hadise album) (Photo credit: Wikipedia)

A genuine “Indian summer” is upon us now with temperatures all over the country in the high thirties and forties. Earlier, Indians used to wear white cotton clothes in summer but now most prefer to dress in synthetic silks, and polyester fabrics, little realising that those clothes are totally inappropriate in this weather.

CLICK & SEE

Even school children — who are issued uniforms with the material and tailoring regulated by the school — end up wearing thick synthetic clothes when ideally they should wear pure cotton or at least a 60 per cent cotton and 40 per cent polyester mix.

To survive, our bodies need to maintain an average internal temperature of 98.6ºF or 36.6ºC and it uses sweating to regulate the temperature. When the outside temperature is high, the body secretes sweat from glands situated in the layer below the skin. The sweat reaches the surface through coiled tubes and forms a thin film of fluid. As this layer evaporates, the body cools down. Sweating can be excessive when the temperature is high, there is increased physical exertion, there is little or no circulation of air and if the clothes are made of synthetic material that traps the sweat. (Nowadays many sports companies manufacture sports clothes out of special material that “wicks” away the sweat).

If sweat pores get blocked (by dead skin cells, dirt or talcum powder), the trapped sweat forms tiny clear bumps below the surface of the skin called miliria crystalline (prickly heat). These look unsightly but do not really cause any symptoms. Eventually, they turn red (miliria rubra), and evolve into a brown scaly rash which can be confused with pimples, folliculitis or chicken pox.

Prickly heat usually appears in covered areas where sweat cannot evaporate easily or the pores are blocked. The forehead is affected if it is covered with a fringe or cap. The upper back and chest, and the arms are other common locations. In adults the rash sometimes appears on the inner thighs or in areas where there are body folds. It is aggravated by friction between the skin and tight fitting non-absorbent synthetic clothing. The continuous rubbing can lead to the skin eventually peeling off, leaving a raw red area.

Prickly heat causes itching and a tingling sensation but scratching can cause secondary infection with bacteria. The appearance of the rash then changes and there can be a yellow pus discharge. The person may develop fever. Uninfected prickly heat, however, does not cause fever. Although prickly heat is uncomfortable and unsightly, with a little care it can be easily prevented.

• Stay away from the direct heat of the sun as far as possible

• Wear loose fitting cotton clothes or at least a 60-40 mix of cotton and polyester

• Make sure school uniforms are stitched out of natural materials, preferably thin materials

• Try to ensure that schools have fans and ventilation.

• Do not scratch. The more you scratch, the more it will itch.

• Use a mild dose of antihistamine to control itching.

• Do not apply thick oil-based creams and talc. They will only block the pores further.

Bathe two or three times a day in tepid water. Add a teaspoon of sodium bicarbonate to a bucket of water before bathing till the prickly heat disappears.

• Use soap containing trichlorhexidine (Dial, Neko) Do not apply soap directly to the skin. Use a moist wash rag, a herbal scrubber or a loofah.

• If prickly heat becomes red and pustular, changes appearance or the temperature rises, consult a doctor immediately.

Contrary to advertisements on television, talc does not soothe, relieve or prevent prickly heat. Talc is made up of finely powdered combinations of ground zinc stearate, and silicates. It blocks the skin pores, increasing the sweat build up and aggravating prickly heat.

Talc causes other medical problems as well. The size of the particles is so small that they can easily be inhaled. The particles can reach the smallest areas of the lung and cause pneumonia, inflammation or swelling of the airways. This can be fatal in babies. If applied to the groin and genital areas, talc can migrate through the vagina, uterus, and fallopian tubes to the ovary. Some scientific studies have found a relationship between the use of talcum powder and cancer of the ovary.

Baby powder is talc based and should not be used. Nappy rash is different from prickly heat and the treatment is different too.

If you get prickly heat, bathe two to three times a day. Use plain calamine lotion (not creams and ointment) to relieve the itching. If secondary infection has occurred, consult a doctor.

You may click to see :
*Remedies for Prickly Heat
*Natural Remedy for Prickly Heat

* Two baths a day keep bacteria at bay

Source : The Telegraph ( Kolkata, India)

Enhanced by Zemanta

Huntington’s Disease

Definition:
Huntington’s disease (also referred to in more formal medical research as Huntington Disease) is an hereditary neurological disorder of the central nervous system that causes progressive degeneration of cells in the brain, slowly impairing a person’s ability to walk, think, talk and reason.

Most people with Huntington’s disease develop signs and symptoms in their 40s or 50s, but the onset of disease may be earlier or later in life. When disease onset begins before age 20, the condition is called juvenile Huntington’s disease. Earlier onset often results in a somewhat different presentation of symptoms and faster disease progression.

….

Medications are available to help manage the symptoms of Huntington’s disease, but treatments can’t prevent the physical, mental and behavioral decline associated with the condition.

It was first described in 1872 by an American doctor, George Huntington, who studied an extended family in Long Island affected by the condition.

Symptoms:
Symptoms of Huntington’s disease commonly become noticeable between the ages of 35 and 44 years, but they can begin at any age from infancy to old age. In the early stages, there are subtle changes in personality, cognition, and physical skills. The physical symptoms are usually the first to be noticed, as cognitive and psychiatric symptoms are generally not severe enough to be recognized on their own at the earlier stages. Almost everyone with Huntington’s disease eventually exhibits similar physical symptoms, but the onset, progression and extent of cognitive and psychiatric symptoms vary significantly between individuals.

The most characteristic initial physical symptoms are jerky, random, and uncontrollable movements called chorea. Chorea may be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slowed saccadic eye movements. These minor motor abnormalities usually precede more obvious signs of motor dysfunction by at least three years. The clear appearance of symptoms such as rigidity, writhing motions or abnormal posturing appear as the disorder progresses. These are signs that the system in the brain that is responsible for movement is affected.[6] Psychomotor functions become increasingly impaired, such that any action that requires muscle control is affected. Common consequences are physical instability, abnormal facial expression, and difficulties chewing, swallowing and speaking. Eating difficulties commonly cause weight loss and may lead to malnutrition.  Sleep disturbances are also associated symptoms. Juvenile HD differs from these symptoms in that it generally progresses faster and chorea is exhibited briefly, if at all, with rigidity being the dominant symptom. Seizures are also a common symptom of this form of HD.

Cognitive abilities are impaired progressively. Especially affected are executive functions which include planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions. As the disease progresses, memory deficits tend to appear. Reported impairments range from short-term memory deficits to long-term memory difficulties, including deficits in episodic (memory of one’s life), procedural (memory of the body of how to perform an activity) and working memory. Cognitive problems tend to worsen over time, ultimately leading to dementia. This pattern of deficits has been called a subcortical dementia syndrome to distinguish it from the typical effects of cortical dementias e.g. Alzheimer‘s disease.

Reported neuropsychiatric manifestations are anxiety, depression, a reduced display of emotions (blunted affect), egocentrism, aggression, and compulsive behavior, the latter of which can cause or worsen addictions, including alcoholism, gambling, and hypersexuality.  Difficulties in recognizing other people’s negative expressions have also been observed. Prevalence of these symptoms is also highly variable between studies, with estimated rates for lifetime prevalence of psychiatric disorders between 33% and 76%.  For many sufferers and their families these symptoms are among the most distressing aspects of the disease, often affecting daily functioning and constituting reason for institutionalisation. Suicidal thoughts and suicide attempts are more common than in the general population.

Mutant Huntingtin is expressed throughout the body and associated with abnormalities in peripheral tissues that are directly caused by such expression outside the brain. These abnormalities include muscle atrophy, cardiac failure, impaired glucose tolerance, weight loss, osteoporosis and testicular atrophy

Reported prevalences of behavioral and psychiatric symptoms in Huntington’s disease :
Irritability 38–73%
Apathy 34–76%
Anxiety 34–61%
Depressed mood 33–69%
Obsessive and compulsive 10–52%
Psychotic 3–11%

Causes:
Huntington’s disease is caused by a single defective gene on chromosome 4. This leads to damage of the nerve cells in areas of the brain including the basal ganglia and cerebral cortex, and to the gradual onset of physical, mental and emotional changes.

The Huntington’s Disease Association estimates between 6,500 and 8,000 people in the UK have the disease.

The tragedy is that by the time symptoms appear, the person has often had a family and may have passed on the gene to their children. Each person whose parent has Huntington’s disease has a 50 per cent chance of inheriting the gene, and everyone who inherits the gene will at some stage develop the disease.

In three per cent of cases, there’s no family history of Huntington’s disease and the genetic fault may be a new mutation.

The disease can’t be prevented from developing if someone has the faulty gene. To inherit the illness, the gene only has to come from one parent, making it autosomal dominant.

The gene for Huntington’s disease can be detected with a blood test, which is available to those aged over 18, before symptoms begin. This can determine whether someone has the faulty gene and help them in their family planning

Risk Factors:
If one of your parents has Huntington’s disease, you have a 50 percent chance of developing the disease. In rare cases, you may develop Huntington’s disease without having a family history of the condition. Such an occurrence may be the result of a genetic mutation that happened during your father’s sperm development.

Complications:
After the onset of Huntington’s disease, a person’s functional abilities gradually worsen over time. The rate of disease progression and duration varies. The time from disease onset to death is often about 10 to 30 years. Juvenile onset usually results in death in fewer than 15 years.

The clinical depression associated with Huntington’s disease may increase the risk of suicide. Some research suggests that the greater risk of suicide occurs before a diagnosis is made and in middle stages of the disease when a person has begun to lose independence.

Eventually, a person with Huntington’s disease requires help with all activities of daily living and care. Late in the disease, he or she will likely be confined to a bed and unable to speak. However, a person’s understanding of surroundings and interactions remain intact for a long time.

Common causes of death include:

*Pneumonia or other infections
*Injuries related to falls
*Complications related to the inability to swallow

Diagnosis:
Medical diagnosis of the onset of HD can be made following the appearance of physical symptoms specific to the disease. Genetic testing can be used to confirm a physical diagnosis if there is no family history of HD. Even before the onset of symptoms, genetic testing can confirm if an individual or embryo carries an expanded copy of the trinucleotide repeat in the HTT gene that causes the disease. Genetic counseling is available to provide advice and guidance throughout the testing procedure, and on the implications of a confirmed diagnosis. These implications include the impact on an individual’s psychology, career, family planning decisions, relatives and relationships. Despite the availability of pre-symptomatic testing, only 5% of those at risk of inheriting HD choose to do so

Clinical:
A physical examination, sometimes combined with a psychological examination, can determine whether the onset of the disease has begun. Excessive unintentional movements of any part of the body are often the reason for seeking medical consultation. If these are abrupt and have random timing and distribution, they suggest a diagnosis of HD. Cognitive or psychiatric symptoms are rarely the first diagnosed; they are usually only recognized in hindsight or when they develop further. How far the disease has progressed can be measured using the unified Huntington’s disease rating scale which provides an overall rating system based on motor, behavioral, cognitive, and functional assessments. Medical imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), only shows visible cerebral atrophy in the advanced stages of the disease. Functional neuroimaging techniques such as fMRI and PET can show changes in brain activity before the onset of physical symptoms.

Grenetic:
Because HD follows an autosomal dominant pattern of inheritance, there is a strong motivation for individuals who are at risk of inheriting it to seek a diagnosis. The genetic test for HD consists of a blood test which counts the numbers of CAG repeats in each of the HTT alleles.[38] A positive result is not considered a diagnosis, since it may be obtained decades before the symptoms begin. However, a negative test means that the individual does not carry the expanded copy of the gene and will not develop HD.

A pre-symptomatic test is a life-changing event and a very personal decision. The main reason given for choosing testing for HD is to aid in career and family decisions. Over 95% of individuals at risk of inheriting HD do not proceed with testing, mostly because there is no treatment. A key issue is the anxiety an individual experiences about not knowing whether they will eventually develop HD, compared to the impact of a positive result.  Irrespective of the result, stress levels have been found to be lower two years after being tested, but the risk of suicide is increased after a positive test result. Individuals found to have not inherited the disorder may experience survivor guilt with regard to family members who are affected. Other factors taken into account when considering testing include the possibility of discrimination and the implications of a positive result, which usually means a parent has an affected gene and that the individual’s siblings will be at risk of inheriting it. Genetic counseling in HD can provide information, advice and support for initial decision-making, and then, if chosen, throughout all stages of the testing process. Counseling and guidelines on the use of genetic testing for HD have become models for other genetic disorders, such as autosomal dominant cerebellar ataxias. Presymptomatic testing for HD has also influenced testing for other illnesses with genetic variants such as polycystic kidney disease, familial Alzheimer’s disease and breast cancer

Embryonic:
Embryos produced using in vitro fertilisation may be genetically tested for HD using preimplantation genetic diagnosis. This technique, where a single cell is extracted from a 4 to 8 cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos with affected HTT genes are not implanted, and therefore any offspring will not inherit the disease. It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the womb.

Differential diagnosis:
About 90% of HD diagnoses based on the typical symptoms and a family history of the disease are confirmed by genetic testing to have the expanded trinucleotide repeat that causes HD. Most of the remaining are called HD-like disorders.  Most of these other disorders are collectively labelled HD-like (HDL). The cause of most HDL diseases is unknown, but those with known causes are due to mutations in the prion protein gene (HDL1), the junctophilin 3 gene (HDL2), a recessively inherited HTT gene (HDL3—only found in one family and poorly understood), and the gene encoding the TATA box-binding protein (HDL4/SCA17). Other autosomal dominant diseases that can be misdiagnosed as HD are dentatorubral-pallidoluysian atrophy and neuroferritinopathy. There are also autosomal recessive disorders that resemble sporadic cases of HD. Main examples are chorea acanthocytosis, pantothenate kinase-associated neurodegeneration and X-linked McLeod syndrome

Treatment:
There’s no cure, but supportive care can ease many symptoms and help a person with Huntington’s disease, and their family, lead as normal a life as possible.

Drugs can relieve symptoms of involuntary movements, depression and mood swings. Speech therapy can help improve speech and swallowing problems. A high-calorie diet can help maintain weight and improve symptoms such as involuntary movement and behavioural problems.

Cognitive changes often result in loss of enthusiasm, initiative and organisational skills, which can make multi-tasking difficult. Constant nursing care is needed in the later stages of the disease and support for carers is important, too.

Secondary illnesses, such as pneumonia, are often the cause of death.

There’s extensive research into possible treatments for Huntington’s disease. One technique is the use of transplants of foetal brain cells, which appear in some cases to repair and rejuvenate the damaged area.

Meanwhile, researchers at the University of Leeds have found that one of the body’s naturally occurring proteins is causing some of the disruption that occurs in the brains of those with Huntington’s, and its effects may be modified by using drugs that are already being used to help cancer patients. But it is likely to be years, if at all, before these developments result in an effective treatment.

Prognosis:
The length of the trinucleotide repeat accounts for 60% of the variation in the age of onset and the rate of progression of symptoms. A longer repeat results in an earlier age of onset and a faster progression of symptoms. For example, individuals with a trinucleotide repeat greater than sixty repeats often develop the disease before twenty years of age, and those with less than forty repeats may not develop noticeable symptoms. The remaining variation is due to environmental factors and other genes that influence the mechanism of the disease.

Life expectancy in HD is generally around 20 years following the onset of visible symptoms.  Most of the complications that are life-threatening result from muscle coordination issues, or to a lesser extent from behavioural changes resulting from the decline in cognitive function. The largest risk is pneumonia, which is the cause of death of one-third of those with HD. As the ability to synchronise movements deteriorates, difficulty clearing the lungs and an increased risk of aspirating food or drink both increase the risk of contracting pneumonia. The second greatest risk is heart disease, which causes almost a quarter of fatalities of those with HD. Suicide is the next greatest cause of fatalities, with 7.3% of those with HD taking their own lives and up to 27% attempting to do so. It is unclear to what extent suicidal thoughts are influenced by psychiatric symptoms, as they may be considered to be a response of an individual to retain a sense of control of their life or to avoid the later stages of the disease.  Other associated risks include choking, physical injury from falls, and malnutrition.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/huntingtons1.shtml

http://en.wikipedia.org/wiki/Huntington’s_disease

http://www.mayoclinic.com/health/huntingtons-disease/DS00401

http://www.healthtree.com/articles/huntingtons-disease/causes/

http://www.bothbrainsandbeauty.com/academic-discussions/huntingtons-disease-991

Enhanced by Zemanta

Human Papilloma Virus (HPV)

Definition:
HPV, short for Human Papillomavirus, is a group of over 100 different kinds of viruses, some of which cause warts on the hands and feet and others which cause genital warts and cervical cancer. This health guide is about the sexually transmitted types of HPV. If you are sexually active, or thinking about becoming sexually active, your best protection is to learn the facts about how HPV is spread and how to prevent getting it.
Click to see the picture
HPV (Human Papillomavirus) is one of the most common sexually transmitted diseases. There are many different types of HPV and more than 30 are sexually transmitted. Researchers keep track of the different types of HPV by identifying them with numbers, such as 6, 11, 16, and 18.

Some sexually transmitted HPV types may cause genital warts. Persistent infection with “high-risk” HPV types—different from the ones that cause skin warts—may progress to precancerous lesions and invasive cancer. HPV infection is a cause of nearly all cases of cervical cancer. However, most infections with these types do not cause disease.

Some types (such as 6 and 11) cause genital warts, others (such as 16 and 18) cause pre-cancerous changes on the cervix that can later lead to cancer of the cervix. In rare cases, the virus can cause other types of cancers to the vulva, vagina, and anus in girls and the anus and penis in guys.

HPV is passed on through genital contact, usually during vaginal and anal sex, as well as during oral sex. People with weakened immune systems, such as those on chemotherapy or people with HIV are more susceptible to HPV infection.

At least 1 in every 2 sexually active young women has had a genital HPV infection. Any sexually active person—no matter what color, race, gender, or sexual orientation—can get HPV. HPV is mainly spread by sexual contact. Very rarely, a mother who is infected with the HPV virus can infect her newborn baby during the delivery.

Symptoms:
It’s estimated that by the age of 27, most sexually active people have been exposed to some strain of HPV, usually without them knowing, and very rarely do doctors know which strain.

Most people with HPV don’t develop symptoms or further health problems, as in around 90 per cent of cases the body’s immune system has naturally cleared it within two years.

However, certain types of HPV (most commonly strains 6, 11, 16 and 18) can cause genital warts in men and women, while other HPV strains (especially 16, 18 and 39) can cause cellular changes that lead to cancer of the cervix and possibly other less common but serious cancers including:

 

•vulval cancer
•cancer of the vagina
•cancer of the penis
•anal cancer
•head and neck (tongue, tonsils and throat) cancers
It’s possible to have HPV present years after sexual contact with an infected person, and it’s also possible to be exposed to more than one strain of HPV.

There is currently no easy way to spot which people affected by HPV exposure will go on to develop cancer or other serious health problems.

Very rarely, a pregnant woman can pass HPV to her baby during birth and the child can develop recurrent respiratory papillomatosis – a chronic lung condition where growths block the airways.

Causes:
*The infected area of your body remains totally normal (called latent or inactive infection). You may never know about it, but you may give the infection to others. Your body then usually clears the infection.

*Bumps, called genital warts, can be seen in your genital area. They almost never lead to cancer.

*Changes in the cells of your cervix can result in an abnormal Pap test. Most of the time, if you are a teenager, your body will clear the HPV and the Pap test will become normal again over several years. However, sometimes the HPV infection persists in your cervix which can lead to cervical cancer. This is why your doctor will want to see you for follow-up visits if you have had an abnormal Pap test.

Risk Factors:
*You had sexual contact at an early age.

*Either you or your sexual partners have had many different sexual partners at any time.

*You or any of your sexual partners have had a history of sexually transmitted diseases.

*Any of your sexual partners did not wear a condom.

HPV and cancer risks:
We don’t fully understand the way in which HPV affects cells. Both high-risk and low-risk strains of HPV can cause the growth of abnormal cells, but only the high-risk types of HPV appear to lead to cancer.

Several types of cancer (up to five per cent worldwide), while linked to other risk factors, are now also associated with HPV exposure:

•cervical cancer (the most common HPV-associated cancer)
•vulval and vaginal cancer (40 to 70 per cent linked to HPV)
•penile cancer (possibly 40 per cent linked)
•anal cancer (around 85 per cent linked)
•cancers of the head and neck (although most are linked to tobacco and alcohol use, it’s now thought about 25 per cent of mouth and 35 per cent of throat cancers may be linked to HPV exposure (in particular HPV strain 16)

Diagnosis:
Sometimes it’s hard to know if you have HPV. Although genital warts are usually seen on, around, or inside your vagina or anus, they may be small and hard to see. And you may not have any symptoms such as pain or bleeding.

In March 2003, the U.S. Food and Drug Administration (FDA) approved a test manufactured by Qiagen, which is a “hybrid-capture” test, as the primary screening tool for detecting HPV cervical infection as an adjunct to Pap testing. The test may be performed during a routine Pap smear. It can detect the DNA of the 18 HPV types that most commonly affect the cervix and distinguish between “low” and “high-risk” HPV types, but it cannot determine the specific HPV types.

According to the National Cancer Institute, “testing samples of cervical cells is an effective way to identify high-risk types of HPV that may be present. The FDA has approved an HPV test as a follow-up for women who have an ambiguous Pap test and, for women over the age of 30, for general cervical cancer screening. This HPV test can identify at least 13 of the high-risk types of HPV associated with the development of cervical cancer. The test can detect high-risk types of HPV even before there are any conclusive visible changes to the cervical cells.”

The recent outcomes in the identification of molecular pathways involved in cervical cancer provide helpful information about novel bio- or oncogenic markers that allow monitoring of these essential molecular events in cytological smears, histological or cytological specimens. These bio- or onco- markers are likely to improve the detection of lesions that have a high risk of progression in both primary screening and triage settings. E6 and E7 mRNA detection PreTect HPV-Proofer, (HPV OncoTect) or p16 cell-cycle protein levels are examples of these new molecular markers. According to published results these markers, which are highly sensitive and specific, allow to identify cells going through malignant transformation.

Other testing:
Although it is possible to test for HPV DNA in other kinds of infections, there are no FDA-approved tests for general screening in the United States or tests approved by the Canadian government, since the testing is inconclusive and considered medically unnecessary.

Genital warts are the only visible sign of low-risk genital HPV, and can be identified with a visual check. These visible growths, however, are the result of non-carcinogenic HPV types. 5% acetic acid (vinegar) is used to identify both warts and squamous intraepithelial neoplasia (SIL) lesions with limited success by causing abnormal tissue to appear white, but most doctors have found this technique helpful only in moist areas, such as the female genital tract. At this time, HPV test for males are only used in research.

Treatment:
There is currently no specific treatment for HPV infection. However, the viral infection, more often than not, clears by itself. According to the Centers for Disease Control and Prevention, the body’s immune system clears HPV naturally within two years for 90% of cases. However, experts do not agree on whether the virus is completely eliminated or reduced to undetectable levels, and it is difficult to know when it is contagious.

Health management is based on prevention, by advising condom use and vaccination.

There is treatment for some of the diseases that HPV can cause, including:

•Genital warts, which can be cauterised or treated chemically.
•Abnormal cervical cells, which can be removed by various techniques.

Treatments for genital warts range from acid medicines, to creams, to laser therapy. The treatment will remove visible warts and unwanted symptoms such as itchiness. The type of treatment your doctor recommends will depend on the number, location and size of the warts and the cost and side effects of the different treatments. It’s important to talk with your health care provider about treatment choices and what type of follow-up you will need. Tell your health care provider if you think you are pregnant so that the right therapy is chosen.

Do NOT use over-the-counter “wart medicine” on genital warts. (These medicines are not meant for the very sensitive skin around your genital area).

Prevention:
Condoms offer some protection against genital infection,  but any exposed skin can transmit the virus. In short, condoms are not 100% effective in preventing HPV. Genital HPV infection is the most frequent sexually transmitted disease in the world.

Vaccines:
Two vaccines are available to prevent infection by some HPV types: Gardasil, marketed by Merck, and Cervarix, marketed by GlaxoSmithKline. Both protect against initial infection with HPV types 16 and 18, which cause most of the HPV associated cancer cases. Gardasil also protects against HPV types 6 and 11, which cause 90% of genital warts.

The vaccines provide little benefit to women who have already been infected with HPV types 16 and 18—which includes most sexually active females. For this reason the vaccine is recommended primarily for those women who have not yet been exposed to HPV during sex. The World Health Organization position paper on HPV vaccination clearly outlines appropriate, cost-effective strategies for using HPV vaccine in public sector programs.

Both vaccines are delivered in three shots over six months. In most countries they are approved only for female use, but are approved for male use in countries like USA and UK. The vaccine does not have any therapeutic effect on existing HPV infections or cervical lesions.

Women should continue to seek cervical screening, such as Pap smear testing, even after receiving the vaccine. Cervical cancer screening recommendations have not changed for females who receive HPV vaccine. Without continued screening, the number of cervical cancers preventable by vaccination alone is less than the number of cervical cancers prevented by regular screening alone.

Both men and women are carriers of HPV. Possible benefits and efficacy of vaccinating men are being studied. According to a study by Harvard University Medical School, to vaccinate boys may not be cost effective, especially if a widespread vaccination of girls continues.

No efficacy trials for children under 15 have been performed. Duration of vaccine efficacy is not yet answered by rigorous methodologic trials. Cervarix efficacy is proven for 7.4 years with published data through 6.4 years while Gardasil efficacy is proven for 5 years. Age of vaccination is less important than the duration of efficacy.

Condoms:-
The Centers for Disease Control and Prevention says that male “condom use may reduce the risk for genital human papillomavirus (HPV) infection” but provides a lesser degree of protection compared with other sexual transmitted diseases “because HPV also may be transmitted by exposure to areas (e.g., infected skin or mucosal surfaces) that are not covered or protected by the condom.”

Studies have suggested that regular condom use can effectively limit the ongoing persistence and spread of HPV to additional genital sites in individuals who are already infected. Thus, condom use reduces the risk that already infected individuals will progress to cervical cancer or develop genital warts.

Microbicides:-
Ongoing research has suggested that several inexpensive chemicals might serve to block HPV transmission if applied to the genitals prior to sexual contact. These candidate agents, known as topical microbicides, are currently undergoing clinical efficacy testing. A recent study indicates that some sexual lubricant brands that use a gelling agent called carrageenan prevent papillomavirus infection in animal model systems. Clinical trial results announced at the 2010 International Papillomavirus Conference indicate that a carrageenan-based personal lubricant called Carraguard is effective for preventing HPV infection in women. The results suggest that use of carrageenan-based personal lubricant products, such as Divine No 9, Bioglide and Oceanus Carrageenan may likewise be effective for preventing HPV infection.

Oral infection:
A review of scientific studies in healthy subjects has found carcinogenic HPV in 3.5% of the studies subjects and HPV16 in 1.3%. Men have higher prevalence of oral HPV than women.

Oral HPV infection is associated with HPV-positive oropharyngeal cancer. Odds of oral HPV infection increases with the number of recent oral sex partners or open-mouthed kissing partners. Nonsexual oral infection through salivary or cross transmission is also plausible

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:

http://www.bbc.co.uk/health/physical_health/conditions/hpv.shtml

http://www.youngwomenshealth.org/hpv.html

http://en.wikipedia.org/wiki/Human_papillomavirus

http://www.hivandhepatitis.com/recent/2009/060909_d.html

http://www.magazine.ayurvediccure.com/what-are-the-health-consequences-of-hpv/

http://w-cancer.com/anal-cancer/

http://e-cervicalcancer.com/human-papilloma-virus-cervical-cancer/

Enhanced by Zemantahttp://bryanking.net/human-papilloma-virus-hpv/

Lomatium dissectum

Botanical Name: Lomatium dissectum
Family: Apiaceae
Tribe: Selineae
Genus: Lomatium
Species: L. dissectum
Kingdom: Plantae
Order: Apiales

Common Name: Fernleaf biscuitroot.

Habitat :It is native to much of western North America, where it grows in varied habitat. It is found in the eastern Transverse Ranges and the Sierra Nevada in California.

Description:
Lomatium dissectum is a perennial herb reaching up to 1.4 meters tall, growing from a thick taproot. The leaves are mostly attached near the base of the plant, spreading with petioles up to 30 centimeters long and large blades divided into many small, narrow segments. The inflorescence is an umbel of many small yellow or reddish flowers, each cluster on a ray up to 10 centimeters long. The fruits resemble pumpkin seeds.

click & see the pictures

Medicinal Uses:
Both Lomatium and Ligusticum were used by Native Americans and early American medical practitioners for a variety of chronic or severe infectious disease states, particularly those of viral origin. Modern research is rather limited, but clinical trials have supported the inclusion of these botanicals for viral infections including HIV and condyloma.  Traditionally it’s demonstrated efficacy against a variety of bacterial infections including tuberculosis.   Lomatium contains an oleoresin rich in terpenes. It acts as a stimulating expectorant, enhancing the liquification and consequent elimination of mucus from the lungs. It also appears to exert a strong antibacterial activity, interfering with bacterial replication and inducing increased phagocytosis. The resin also contains a number of furanocoumarins including nodakenetin, columbianin and pyranocoumarin. These resins may be responsible for the plant’s antiviral effect. They may also be partly responsible for the phagocytic action lomatium causes.

Based on empirical evidence and discussions with clinical herbalists, lomatium can be used as an antimicrobial, especially in the lungs and upper respiratory tract. It provides quick-acting relief in cases of viral or bacterial infection, particularly when there is a large amount of thick or sticky mucus and infection is deep-seated and persistent. Consider taking lomatium for pneumonia, infective bronchitis and tuberculosis.

As an immunostimulant, this herb is traditionally used to treat colds and flus. Many cases during the 1920s U.S. influenza epidemic were successfully treated with lomatium by the professional herbalists of the time, and it has been used for this purpose by Native Americans since the introduction of influenza to the Americas.  Its infection-fighting ability makes lomatium valuable as a mouthwash and gargle for oral and throat infections, as a douche for bacterial and viral infections or candida, as a skin wash for infected cuts or wounds, and in many other first- aid situations.  Both tea and tincture forms are commonly used. For acute bacterial or viral infections, 2.5 ml of the tincture diluted in water can be used three to four times daily. A painful, itchy full-body rash that can persist for days occurs frequently when the crude tincture is used.  It seems to occur more commonly with the strong, fresh-root preparation and disappears when treatment stops.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:

http://en.wikipedia.org/wiki/Lomatium_dissectum

http://plants.usda.gov/java/profile?symbol=LODI&photoID=lodi_006_ahp.jpg

http://www.herbnet.com/Herb%20Uses_AB.htm

Enhanced by Zemanta

Aristolochia debilis

Botanical Name :Aristolochia debilis
Family: Aristolochiaceae
Subfamily: Aristolochioideae
Genus: Aristolochia
Species: Aristolochia debilis
Regnum: Plantae
Cladus: Angiosperms
Cladus: Magnoliids
Order: Piperales

Synonyms : A. recurvilabra. Hance.

Common Name :Birthwort, Frail

Habitat : E. Asia – China, Japan. Roadside thickets and meadows in lowland, C. and S. Japan and in China.

Description:
Aristolochia debilis is a perennial herb growing to 1 m (3ft 3in) by 1 m (3ft 3in).
It is hardy to zone 8. It is in flower from Jul to August, and the seeds ripen from Sep to October. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Flies.

You may click to see the pictures
..
The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and requires well-drained soil.The plant prefers acid, neutral and basic (alkaline) soils..It can grow in semi-shade (light woodland) or no shade.It requires moist soil.

Cultivation:
Prefers a well-drained loamy soil, rich in organic matter, in sun or semi-shade. Succeeds in ordinary garden soil. This species is not very hardy in Britain, tolerating temperatures down to about -5°c. Most species in this genus have malodorous flowers that are pollinated by flies.

Propagation:
Seed – best sown in a greenhouse as soon as it is ripe in the autumn. Pre-soak stored seed for 48 hours in hand-hot water and surface sow in a greenhouse. Germination usually takes place within 1 – 3 months at 20°c. Stored seed germinates better if it is given 3 months cold stratification at 5°c. When large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for their first winter. Plant out in late spring or early summer after the last expected frosts. Division in autumn. Root cuttings in winter[

Edible Uses:Leaves are edible.They are cooked. It is said that the leaves of this species are not poisonous but caution is advised.

Medicinal Uses:
Alterative;  Anodyne;  Antibacterial;  Antifungal;  AntiinflammatoryAntitussiveCarminative;  Cytotoxic;  Diuretic;  Expectorant;  Hypotensive;
Stomachic;  Tonic.

Alterative, antibacterial, antifungal, diuretic. Stimulates energy circulation. The fruit and its capsule are antiasthmatic, antiseptic, antitussive and expectorant. It is used internally in the treatment of asthma and various other chest complaints, haemorrhoids and hypertension. The root is anodyne and anti-inflammatory. It is used internally in the treatment of snakebite, gastric disorders involving bloating, and is clinically effective against hypertension. It is harvested in the autumn and dried for later use. The whole plant is antitussive, carminative, stimulant and tonic. The root contains aristolochic acid. This has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy. Aristolochic acid can also be used in the treatment of acute and serious infections such as TB, hepatitis, liver cirrhosis and infantile pneumonia. It also increases the cellular immunity and phagocytosis function of the phagocytic cells. Aristolochic acid is said to be too toxic for clinical use

Internally used for arthritis, purulent wounds, hypertension, snake and insect bites, and gastric disorders involving bloating (roots); for asthma, wet coughs, bronchitis, hypertension and hemorrhoids (fruits). Indications: heat in the lungs manifested as cough with profuse yellow sputum and asthma.  The fruit (Madouling) is used with Loquat Leaf, Peucedanum root, Mulberry bark and Scutellaria root.  Deficiency of the lungs manifested as cough with scanty sputum or with bloody sputum and shortness of breath.  Fruit is used with Glehnia root, Ophiopogon root, Aster root and Donkey hide gelatin.

Known Hazards: No specific details for this species is known  but most members of this genus have poisonous roots and stems. The plant contains aristolochic acid, this has received rather mixed reports on its toxicity. According to one report aristolochic acid stimulates white blood cell activity and speeds the healing of wounds, but is also carcinogenic and damaging to the kidneys. Another report says that it is an active antitumour agent but is too toxic for clinical use. Another report says that aristolochic acid has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy and that it also increases the cellular immunity and phagocytosis function of the phagocytic cells

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:

http://www.pfaf.org/user/Plant.aspx?LatinName=Aristolochia%20debilis

http://www.herbnet.com/Herb%20Uses_AB.htm

http://species.wikimedia.org/wiki/Aristolochia_debilis

http://www.exot-nutz-zier.de/images/prod_images/Aristolochia_debilis.jpg

http://www.georgiavines.com/cart/index.php?main_page=product_info&cPath=9_10&products_id=118

http://www.asianflora.com/Aristolochiaceae/Aristolochia-debilis.htm

Enhanced by Zemanta